Postmortem measurements of thyroid hormones in blood and vitreous humor combined with histology.

The aim of this study was to investigate whether clinical reference premortem values can be used to assess postmortem concentrations of thyroxine, triiodothyronine, and thyroid stimulating hormone (TSH), to compare the postmortem concentrations in blood and vitreous humor, and to study the possibility of diagnosing hyperthyroidism by comparing thyroid histologic appearance and postmortem hormone values. Biochemical analyses of free thyroxine (FT4), free triiodothyronine (FT3), and TSH in femoral blood and vitreous humor were made in 38 cases. In 40 cases, the hormones and thyroid histologic appearance were studied; 22 had no significant pathologic changes, and 18 showed focal hyperplasia of the follicular epithelium. A positive correlation was seen between the femoral blood and vitreous humor concentrations of FT4 (R = 0.66) but not between the corresponding concentrations of FT3 and TSH. A positive correlation was also seen between FT3 and FT4 in femoral blood (R = 0.74). In cases with normal thyroid histologic appearance, 58% were found to have FT4 values >24 pmol/L (clinical reference interval 9-24 pmol/L), mean value 27.5 +/- 9.4 pmol/L), which did not differ from the FT4 values in the cases with hyperplasia, 31.6 +/- 15 pmol/L. Only 5% of the T3 measurements in the group with normal histologic appearance were >9 pmol/L (clinical reference interval 3-9 pmol/L). The mean value of FT3 in cases with normal histologic appearance was 3.4 +/- 1.3 pmol/L, and in the group with hyperplasia 8.6 +/- 6.1 pmol/L. The difference was statistically significant P < .005). It is concluded that postmortem values of FT3 and FT4 in femoral blood are fairly comparable to premortem clinical reference values, but the upper normal limit, especially for T4, has to be adjusted upward. Analysis of vitreous humor cannot be used post mortem to assess thyroid function. Histologically, hyperplastic changes correlate well with elevated FT3 in femoral blood.     

Preliminary study of the effect of acute antemortem haemorrhage on postmortem abdominal impedance in rats

Studies over many years have revealed a consistent, inverse relationship between extracellular impedance of the rat abdomen and postmortem interval (PMI). Recent studies have shown that this relationship can be improved by correcting measured impedances to their theoretically predicted values at an arbitrarily chosen temperature of 40 degrees C, thus rendering them independent of the tissues' temperature at the time of impedance measurement. The present study, undertaken as a part of an ongoing effort to identify variables which might influence postmortem rate of change in abdominal impedance, was aimed at studying the possible effect of acute antemortem haemorrhage on abdominal impedance. Sudden loss of approximately 30% of the total blood volume, immediately prior to the death was without statistically significant effect on the pattern of postmortem change in abdominal impedance. Thus, in the control and experimental rats, respectively, impedance decreased progressively from 58.7 +/- 1.8 and 68.0 +/- 11.3 omega, 1 h postmortem, to 31.5 +/- 2.2 and 33.7 +/- 4.7 omega at a postmortem interval of 120 h (n = 6 in each group). In both groups, the relationship between impedance and postmortem interval was either linear or curvilinear. These findings are believed to mitigate in favour of continued effort to examine the potential usefulness of abdominal impedance, as an index of postmortem interval, under conditions encountered in routine forensic investigation.     

Postmortem vitreous humor beta-hydroxybutyrate: its utility for the postmortem interpretation of diabetes mellitus

Ketoacidotic coma is one of the most serious complications arising from diabetes mellitus, especially type I, and may be the cause of sudden death especially in diabetes type I. Since beta-hydroxybutyrate (beta-OHB) serum concentrations might provide more information on the severity of ketoacidosis, the aim of this study was to evaluate the concentrations of beta-OHB in vitreous humor and its correlation with other biochemical parameters during postmortem examination. We intended to ascertain the sensitivity and the specificity of these markers for diagnosing diabetes mellitus and the presence of ketoacidosis. This study involved 453 cadavers with a mean age of 57.6 years (S.D. 20.7) and a mean postmortem interval of 17.8 h (S.D. 9.6, range 2-61 h). Cases were assigned to two diagnostic groups according to the antemortem diagnosis of diabetes mellitus, based on the patients' medical records. In vitreous humor statistically significant differences were found in biochemical marker concentrations between the two diagnostic groups, the highest values being obtained in the group of subjects with a previous diagnosis of diabetes mellitus. The measurement of beta-OHB in vitreous humor may be a useful alternative to using blood during postmortem analysis. The presence of high levels of beta-OHB may help interpret the cause of death in diabetics when the autopsy result is negative.     

Amount of postmortem bleeding: an experimental autopsy study

An experimental autopsy study was performed on 64 cases (55 male, 9 female; average age 51.5 +/- 16.2 years) of sudden natural (38 cases) and asphyxic deaths (26 cases). The study objective was the amount of postmortem bleeding from postmortem cutting of the thoracic aorta, related to the time since death. The amount of postmortem bleeding ranged from 100 to 1300 cm, 440.6 +/- 268.1 cm on average. The time since death up to the autopsy time ranged from 4 to 72 hours, 19.4 +/- 12.9 in average. A statistically significant correlation between the amount of postmortem bleeding and postmortem time interval was stated: Pearson correlation test value r = -0.461 (P = 0.000): the shorter the time interval, the larger the amount of bleeding. The formula of linear regression was estimated according to this correlation: amount of postmortem bleeding (cm) = -9.571 x time since death (h) + 626.659. This proves that the amount of postmortem bleeding (eg, from aortic blunt rupture) could be about 620 cm.     

Estimation of postmortem interval. Temperature-correction of extracellular abdominal impedance during the first 21 days of death

Extracellular impedance of the intact abdomen of rats increased from 79.0+/-7.4Omega, 1h postmortem (i.e. 0.04 day), to 130.5+/-14.4Omega at postmortem interval (PMI)=1 day. Impedance then decreased with time, reaching 64.2+/-9.9Omega at PMI=21 days. The time taken for mean abdominal impedance to decrease below the value at PMI=0.04 day averaged 16 days. It is therefore impossible, using extracellular abdominal impedance alone, to distinguish (in terms of interpolating PMI) between numerically equal impedances on the rising and falling phases of curves depicting impedance as a function of PMI.Correction of measured impedances to their theoretically-predicted values at an arbitrarily chosen temperature of 40 degrees C appreciably diminished the magnitude of the increase in impedance following death. Thus, temperature-corrected abdominal impedance increased from 56.2+/-4.8Omega at PMI=0.04 day to 59.5+/-6.2Omega at PMI=1 day. Impedance then decreased, reaching 29.2+/-4.1Omega at PMI=21 days. The time taken for mean, temperature-corrected abdominal impedance to decrease below the value at PMI=0.04 day averaged 3 days (as opposed to 16 days (see above) in the absence of temperature-correction).These findings are believed to improve the usefulness of extracellular abdominal impedance as a potential tool for estimation of postmortem interval.     

Temperature-correction of abdominal impedance: improved relationship between impedance and postmortem interval

The relationship between extracellular abdominal impedance and postmortem interval (PMI) reflects the combined effects, on impedance, of postmortem cooling of the tissues and of autolysis per se. This study was performed in order to eliminate temperature change as a major factor contributing to the time course of postmortem change in abdominal impedance. Dissociation of thermal and autolytic influences was achieved by recording deep abdominal temperature at the time of impedance measurement, followed by correction of all measured impedances to their theoretically predicted values at an arbitrarily chosen temperature of 40 degrees C. Uncorrected abdominal impedance increased from 82+/-12 Ohmz, 1 h after death, to 108+/-21 Ohmz after 12 h. Impedance then decreased to 96+/-23, 89+/-22, 75+/-19, 66+/-21 and 59+/-19 Ohmz at postmortem intervals of 24, 36, 48, 60 and 72 h, respectively. In contrast, corrected abdominal impedance decreased progressively from 63+/-7 Ohmz, 1 h after death, to 61+/-9, 56+/-11, 51+/-10, 46+/-10, 39+/-11 and 35+/-10 Ohmz at postmortem intervals of 12, 24, 36, 48, 60 and 72 h, respectively. The improved relationship between (corrected) abdominal impedance and PMI is of potential value in estimating time since death.     

Vitreous humor biochemical constituents: evaluation of between-eye differences

The present study was conducted to investigate the differences in the vitreous humor biochemical concentrations for vitreous electrolytes and calcium in the same pair of eyes at identical postmortem interval (PMI). The vitreous humor samples were collected independently in both eyes from 48 autopsies (PMI range, 4.5-84.3 hours) with documented time of death. The samples were analyzed for potassium, sodium, chloride, and calcium using a Beckman Coulter LX20 Automated Analyzer based on ion-selective electrode methodology. There were no statistically significant between-eye differences at identical postmortem interval. A significantly high correlation was observed between paired potassium concentrations of both the eyes. A highly significant linear correlation was observed between the individual eye and mean potassium concentrations of both the eyes with postmortem interval. The observed differences were not significantly correlated with postmortem interval. The results demonstrated that the between-eye differences for vitreous electrolytes and calcium are insignificant. Therefore, the utility of vitreous biochemistry, particularly potassium in postmortem interval estimation and other forensic applications, cannot be questioned solely on the basis of these differences.     

死后血浆和溶血样本中IgE的稳定性

目的 探究死后血浆和溶血样本中免疫球蛋白E(immunoglobulin E,IgE)经过不同保存条件及冻融处理后的稳定性.方法 选取39例死后48 h内非冷冻尸体的心血样本,其中20例取血浆样本,19例取全血制成溶血样本.将样本置于-20℃、4℃、25℃条件下保存28 d及-80℃条件下保存1年以探究IgE在不同保存...     

The extent of postmortem drug redistribution in a rat model.

The aim of this study was to investigate the postmortem redistribution of several drugs in a rat model and to examine if any of the pharmacological properties was related to the extent of this phenomenon. One of the following drugs: phenobarbital (phenobarbitone), acetaminophen (paracetamol), carbamazepine, codeine, verapamil, amphetamine, mianserin, trimeprazine (alimemazine) or chloroquine was administered together with nortriptyline orally to rats 90 min prior to sacrifice. Heart blood was sampled immediately before sacrifice and after 2 h postmortem, as it has previously been shown that this is sufficient time for postmortem concentration changes to occur in heart blood. Blood was also sampled from the clamped abdominal inferior vena cava (representing peripheral blood) and tissue samples were taken from lungs, myocardium, liver, kidney, thigh muscle, forebrain, and vitreous humor together with a specimen from the minced carcass. Drugs were analyzed by high performance liquid or gas chromatography. For phenobarbital, acetaminophen and carbamazepine the postmortem to antemortem blood drug concentration ratios were close to 1.0 and tissue concentrations were low. The postmortem to antemortem heart blood drug concentration ratio for chloroquine (6.9 +/- 1.5) was higher than for nortriptyline (3.5 +/- 0.3), and the remaining drugs (codeine, verapamil, amphetamine, mianserin, and trimeprazine) showed ratios of the same magnitude as nortriptyline. The postmortem to antemortem blood drug concentration ratios for both heart blood and blood from the vena cava and also the lung to antemortem blood drug concentration ratio were closely related to the apparent volume of distribution for the drugs studied (p < 0.001). Accordingly, an apparent volume of distribution of more than 3-4 L/kg is a good predictor that a drug is liable to undergo postmortem redistribution with significant increments in blood levels. The postmortem drug concentration in blood from vena cava was closely related to the antemortem blood level, confirming that among the postmortem samples, the peripheral blood sample was the most representative for the antemortem blood concentration.     

钾中毒死亡家兔的尸体化学变化

目的研究家兔钾中毒死亡后的尸体化学变化特征,为钾中毒的法医学鉴定提供参考。方法采用浓度为0.3%和1%的KCl葡萄糖溶液分别以全速和100滴/min的速度输给家兔,至其死亡,测定家兔输液前后血、尿电解质浓度,比较两种不同输液方式所致钾中毒死亡后尸体化学变化特征。结果输钾前后,家兔血清K (SK)浓度升高,血清Na 、Ca2 、Cl-及HCO3-浓度均降低,全血K (TK)及血清Mg2 浓度变化无显著性差异。0.3%KCl组致死输液时间长于1%组(P=0.006),致死输钾量无显著性差异(P=0.062);TK、血清Na 、Mg2 及Cl-浓度变化值具有显著差异,SK、Ca2 、HCO3-浓度变化值无显著差异;尿量和尿液各电解质浓度指标未见显著性差异。结论尸体SK、TK及血清Mg2 浓度升高,有助于钾中毒的法医学死后诊断。     

Digoxin, magnesium, and potassium levels in a forensic autopsy material of sudden death from ischemic heart disease

In 91 cases where the cause of death was heart disease, digoxin, Mg and K concentrations in serum and ventricular myocardium were measured post mortem. Forty per cent were positive for digoxin in both serum and myocardium. The mean serum level was 5.1 +/- 2.4 nmol/l and the mean myocardial level was 42.6 +/- 27.5 ng/g. Correlation could be established between serum and myocardial concentrations of digoxin. There were statistically significant differences in serum as well as in myocardial digoxin levels in persons on 0.13 mg and 0.25 mg per day, respectively. Myocardial levels of Mg and K were low as generally found in persons with ischemic heart disease. There was no correlation between these levels and myocardial digoxin concentrations. Caution must be exercised in the assessment of digoxin results from cadaver samples because of the postmortem rise of digoxin serum concentrations. Considering this fact, the results still indicate that the prevalence of toxic digoxin concentrations might be more common than previously thought.     

Biochemical measurements of glucose metabolism in relation to cause of death and postmortem effects

This study was performed to examine the relationship between postmortem biochemical values and cause of death. The follow samples were taken from 399 corpses: cerebrospinal fluid (CSF; n = 376, suboccipital), blood (n = 158, femoral vein), and urine (n = 101, at autopsy). (See Table 1 for causes of death) All samples were stored at -80 degrees C. A further 100 samples of blood were later taken and stored at +4 degrees C before testing. Biochemical determinations made were: glucose in CSF, blood, and urine (hexokinase method); lactate (LDH/GPT) and free acetone (HS-gas chromatography) in CSF; hemoglobin A1 in blood (microcolumn technique). In 34 cases fatal diabetic coma was considered verified by morphological and chemical findings. One hundred cases of sudden cardiac death were chosen as the main control group. In 32 of the 34 cases defined above, the value of the formula of Traub (glucose + lactate in CSF) exceeded 415 mg/dl. It is not influenced significantly by hyperglycemia or hyperlactatemia due to factors other than diabetes (i.e., carbon monoxide, asphyxia). After death the value rose till the 30th hpm, then remained stable for at least 1 week. Fatal coma was defined as the ketoacidotic form if free acetone in CSF ranged above 21 mg/l. In these cases, CSF glucose and free acetone correlated positively. Hemoglobin A1 remained stable after death. Its amount was independent from postmortem blood glucose, postmortem interval and total hemoglobin. Furthermore, the manner of storage (-80 degrees or +4 degrees C) had no significant influence on its values. In 29 of 34 cases of fatal coma, Hb A1 exceeded 12.1%. Analysis of urine glucose showed elevated levels (over 500 mg/dl) in diabetic comas. On conclusion, fatal diabetic coma seems indicated as the cause of death if measured values of postmortem biochemistry exceed the following limits: CSF-Traub 415 mg/dl, free acetone (CSF) 21 mg/l; Hb A1 12.1%; urine glucose 500 mg/dl. Most important are the Traub formula and hemoglobin A1. Usually, in fatal coma both values are elevated. If both of them are normal, diabetic coma can nearly be excluded. Combined evaluation of all values is absolutely necessary. Morphology must also always be taken into account. Consequently, a diagnosis of fatal coma can be obtained by a process of elimination.     

The relationship between alcohol elimination rate and increasing blood alcohol concentration--calculated from two consecutive blood specimens

In the period 1991-2005, a blood-alcohol concentration (BAC) analysis was carried out at the Institute of forensic medicine in Novi Sad including 2023 two consecutive blood specimens using the Headspace Gas Chromatography method. Cases with no alcohol concentration values, as well as cases where blood samples were taken within 1 h after the criminal act, were not taken into consideration. Following this rule, 1198 cases were considered in this study and all samples were grouped in 29 ranges of BAC1 of delta(BAC) = 0.1 g/kg, starting from 0.1-0.19 g/kg to 2.9-2.99 g/kg of absolute alcohol. Gathered results and elimination curve differ from the zero-order model of elimination proposed by Widmark and point to an elimination process similar to a well-known Michaelis-Menten elimination kinetics model and its variants. Results reported in this study show dependence of alcohol elimination rate (beta-slope) and BAC value. The analysis of beta60-slope versus BAC shows that a correlation between beta60 (y) and BAC (x) has a logarithmic trend line. The value of alcohol elimination rate shows a slight increment with increase of BAC alcohol, with the mean value of beta60 = 0.221 +/- 0.075 g/kg. Differences in values of beta60 among consecutive intervals of delta(BAC) = 0.1 g/kg are not significant (p>0.05). When obtained samples were grouped into ranges of 0.5 g/kg each in these intervals beta60 had the following values by range: 0.1-0.49 g/kg = 0.139 g/kg +/- 0.035; 0.5-0.99 g/kg = 0.184 g/kg +/- 0.043; 1-1.49 g/kg = 0.213 g/kg +/- 0.052; 1.5-1.99 g/kg = 0.239 g/kg +/- 0.058; 2-2.49 g/kg = 0.265 g/kg +/- 0.073; 2.5-2.99 g/kg = 0.306 g/kg +/- 0.096. Differences in values of beta slope among consecutive intervals of delta(BAC) = 0.5 g/kg are significant (p<0.01). The elimination curve in the BAC interval 0.5-2.5 g/kg has a linear trend, while beta-slope (y)/BAC (x) correlation is given as beta60 = 0.15 g/kg + (0.05 g/kg x BAC). Retrograde calculation of the blood alcohol concentration in tempore criminis (BAC(tc)) based on the determined alcohol concentration in the blood specimen (BAC(t)) shows a statistically significant difference between BAC(tc) calculated using a standard zero-order model versus corrected methodology. The higher the BAC(t) and the longer the calculation time, the greater and statistically more significant (p<0.01) is the difference between the calculated values of BAC(tc).     

K~+/Na~+比值与损伤时间的关系

本文使用原子吸收光谱法测定12只大鼠36个烧伤局部肌肉标本的 K~+/Na~+值,检测结果:生前60、 30、 15min 以及死后20min 肌肉标本的 K~+/Na~+值比对照组分别下降:69～94％(平均86％)、56～89％(平均77％)、47～82％(平均71％)、4～38％(平均27％),此结果经统计学处理,表明生前伤与死后伤的 K~+/Na~+比值的下降率有明显差异。同时发现生前损伤的各实验组随存活时间的延长,K~+/Na 比值的下降率有增加的倾向。笔者认为,此方法是烧伤时间推断的一种简便,可靠的方法,对法医学实践有一定实用价值。     

A large-scale study of the relationship between blood and breath alcohol concentrations in New Zealand drinking drivers

Blood alcohol concentrations (BAC) and corresponding breath alcohol concentrations (BrAC) were determined for 21,582 drivers apprehended by New Zealand police. BAC was measured using headspace gas chromatography, and BrAC was determined with Intoxilyzer 5000 or Seres Ethylometre infrared analysers. The delay (DEL) between breath testing and blood sampling ranged from 0.03 to 5.4 h. BAC/BrAC ratios were calculated before and after BAC values were corrected for DEL using 19 mg/dL/h as an estimate of the blood alcohol clearance rate. Calculations were performed for single and duplicate breath samples obtained using the Intoxilyzer (groups I-1 and I-2) and Seres devices (groups S-1 and S-2). Before correction for DEL, BAC/BrAC ratios for groups I-1, I-2, S-1, and S-2 were (mean+/-SD) 2320+/-260, 2180+/-242, 2330+/-276, and 2250+/-259, respectively. After BAC values were adjusted for DEL, BAC/BrAC ratios for these groups were (mean+/-SD) 2510+/-256, 2370+/-240, 2520+/-280, and 2440+/-260, respectively. Our results indicate that in New Zealand the mean BAC/BrAC ratio is 19-26% higher than the ratio of the respective legal limits (2000).     

Systematic analysis of stutter percentages and allele peak height and peak area ratios at heterozygous STR loci for forensic casework and database samples

To assist the interpretation of STR DNA typing results from forensic casework samples containing mixtures, the range of heterozygous allele peak height and peak area ratios (HR) and stutter percentages (stutter %) for the loci comprised in the AmpFlSTR Profiler Plus (PP) kit were assessed on 468 database and 275 casework single source samples. Stutter % medians were similar for database and casework samples, ranging from 2% to 7%. The upper limit of the stutter value range was 16%, calculated as median +3 SD, although lower locus-specific values could be used. HR medians were 93 +/- 6.5% for database samples, 88 +/- 12% for casework samples. For casework samples, the maximum signal imbalance noted was 52%, calculated as median -3 SD. No significant difference was observed between peak height and peak area calculated values. This study shows the importance of selecting the proper reference database for the establishment of HR threshold values.     

Heart fatty acid binding protein as a marker for postmortem detection of early myocardial damage

Depletion of heart fatty acid binding protein (H-FABP) from cardiomyocytes with varying post-ischemia intervals was studied in acute myocardial infarction (AMI) model of rat, and 22 human autopsy cases were studied with streptavidin-peroxidase conjugated method (S-P). It was observed that as early as 15 min after ischemia, the depletion of H-FABP could be detected in model rats. With the ischemic time prolonged, the depletion of H-FABP was more and more evident. In all human cases with myocardial infarction, absent H-FABP staining could be found in infarcted area. And in some suspected early myocardial infarction cases, depletion of H-FABP staining could be demonstrated in areas that showed normal hematoxylin-eosin (HE) staining. The blood samples from model rats before ligation, at varying post-ischemia intervals and various postmortem time were measured for plasma concentration of H-FABP with enzyme-linked immuno-sorbent assay (ELISA) method. At 15 min after myocardial ischemia, the concentration of H-FABP was 4 times higher (546.0+/-85.3 microg/l) than that of the baseline level (103.7+/-94.1 microg/l). With the continuation of ischemic time, the concentration of H-FABP increased and peaked at 4 h (1953.5+/-405.3 microg/l), then decreased. The plasma concentration of H-FABP decreased slightly with postmortem time, but was still significant higher at any postmortem intervals than that of baseline level within 48 h after death. The results suggest that H-FABP staining can detect very early ischemic damages in human myocardium and the elevated plasma concentration of H-FABP in rat was an indicator of AMI, which was not affected by autolysis.     

A blood cyanide distribution study in the rabbits intoxicated by oral route and by inhalation

Blood cyanide concentration was determined in rabbits intoxicated orally or by inhalation. Experiments were carried out under urethane anaesthesia. In the inhalation experiments, rabbits inhaled a combustion product containing HCN via the tracheal cannula and in the oral studies animals were administered NaCN solution into the stomach. In addition to the carotid artery and jugular vein blood samples, postmortem samples were obtained from both sides of the heart and the descending vena cava. The arterial cyanide concentration in the inhalation group showed a close relationship with ventilation. After an initial rise, blood levels decreased a little, in some cases with transient apnea. At the last stage it again increased with gasping, reaching its maximal value. After ultimate apnea, the blood cyanide concentration declined. The blood cyanide values were higher in the oral group than in the inhalation group. The difference between the two groups became larger in the inferior order, the left heart blood--the right heart blood--blood in the descending vena cava. The left heart/right heart ratio of the inhalation group was significantly higher than that of the oral group (1.28+/- 0.28 vs. 0.95+/- 0.09). The coefficient of variation (c.v.) of the inhalation group was larger than that of the other group. Within the inhalation group, the left heart blood showed the largest c.v. values and this was probably due to redistribution of the cyanide by bloodstream after attainment of the maximal concentration.     

Interpretation of postmortem digoxin levels: evaluating a "corrective factor" for postmortem blood digoxin concentration

Interpretation of postmortem serum digoxin levels is made difficult above all by a possible prefinal or postmortem rise in digoxin concentrations in the blood. To compensate for this postmortem increase, Eriksson et al. (1984) divided the level of postmortem digoxin in femoral venous blood by a factor of 1.5; in the opinion of these authors, postmortem digoxin levels still exceeding "therapeutic levels" after division by 1.5 are an index of digoxin overdose. The diagnostic value of this "correction factor" was investigated. In 56 cases with documented digoxin medication, samples of postmortem femoral venous blood were taken and the level of digoxin determined. In none of the cases had there been a clinical diagnosis of digoxin intoxication. Fifty percent of the measured values were above "therapeutic levels" (0.7 ng/ml to 2.2 ng/ml). Following division by 1.5, 20% of the cases still showed levels exceeding 2.2 ng/ml; the highest "corrected" value was 4.44 ng/ml. Taking into account the length of time between final dosage and death, individual differences in sensitivity to digitalis glycoside, and the complexity of ante- and postmortem dispersion processes, we concluded for the cases we studied that an (undetected) digoxin overdose was not even likely in those cases whose postmortem values after division by 1.5 lie above "therapeutic levels". The "correction factor" proposed by Eriksson et al. (1984) is only of limited diagnostic value; at best the "corrected" values can give an approximate indication of the corresponding antemortem serum digoxin concentrations. In particular, "corrected" values only a little above "therapeutic levels" could not confirm suspicion of an overdose with sufficient certainty.     

Clinical and forensic examinations of glycemic marker 1,5-anhydroglucitol by means of high performance liquid chromatography tandem mass spectrometry

Postmortem diagnosis of diabetes and a diabetic coma can be difficult because of the lack of characteristic morphological findings. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for reabsorption in the kidneys. Therefore, diabetics with a permanent hyperglycemia show significantly lower serum concentrations of 1,5-AG than non-diabetics. A liquid chromatography-mass spectrometric method for the determination of 1,5-AG in serum and postmortem blood was developed and validated according to international guidelines. Linearity was given between 1μg/ml and 50μg/ml. Recovery rates ranged between 70.8% and 89.8%, the limit of quantification of the procedure was 0.20μg/ml, limit of quantification was 0.55μg/ml. Serum of 199 diabetics and 116 non-diabetics and femoral blood of 31 diabetic and 27 non-diabetic deceased was measured. Average concentrations were significantly (p<0.001) higher in non-diabetics compared to diabetics ante and postmortem. Seven of the diabetics may have died because of a hyperglycemic coma indicated by a sum formula of Traub>450mg/dl. 1,5-AG average concentrations in these deceased were not significantly different to diabetics which did not die because of a diabetic coma. Concentrations of 1,5-AG give a hint for not well controlled diabetes antemortem and postmortem and can be assumed as an additional and alternative information postmortem to the measurement of HbA1c or fructosamine.